Previous work by the applicant suggested that in ferrets, as in monkeys and man, a perinatal period exists during which exposure to androgen causes behavioral masculinization. However, in none of these species has a perinatal period yet been identified during which androgenization causes behavioral defeminization. Experiments are proposed which will search further for defeminizing effects of perimatally administered sex steroids on ferrets' coital behavior, and which explore the possible contribution of two metabolites of testosterone (T), estradiol (E2) and 5a-dihydrotestos-terone (DHT), to the differentiation of masculine coital behavior and socio-sexual orientation in this species. These studies will: (1) measure plasma levels of T in ferrets of both sexes during perinatal life, (2) attempt to induce behavioral defeminization in female ferrets by giving T during perinatal periods other than those previously studies, (3) compare the ability of T, E2, and DHT to cause the development of masculine coital behavior and of a preference to approach the estrous female, and test the ability of various drugs which inhibit the formation or neural binding of E2 and DHT to block behavioral masculinization in normal males, and (4) determine whether estrogen or androgen binding molecules are present perinatally in cytosol fractions prepared from ferret hypothalamus + preoptic region of each sex. Previous research also indicated that metabolites of T, (E2 and DHT) formed in the forebrain may normally contribute to the activation of sexual behavior in the male rat, perhaps in part by facilitating functional activity in ascending dopaminergic neurons.